The Journal of Experimental Medicine
BioLegend: Antibody Reagents
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Published online January 22, 2007
doi:10.1084/jem.20061801
The Journal of Experimental Medicine, Vol. 204, No. 2, 259-265
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Gourzi et al.
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BRIEF DEFINITIVE REPORT

 Viral induction of AID is independent of the interferon and the Toll-like receptor signaling pathways but requires NF-{kappa}B

Polyxeni Gourzi, Tatyana Leonova, and F. Nina Papavasiliou

Laboratory of Lymphocyte Biology, The Rockefeller University, New York, NY 10021

CORRESPONDENCE F. Nina Papavasiliou: papavasiliou{at}rockefeller.edu

Activation-induced cytidine deaminase (AID) is expressed in germinal centers of lymphoid organs during immunoglobulin diversification, in bone marrow B cells after infection with Abelson murine leukemia retrovirus (Ab-MLV), and in human B cells after infection by hepatitis C virus. To understand how viruses signal AID induction in the host we asked whether the AID response was abrogated in cells deficient in the interferon pathway or in signaling via the Toll-like receptors. Here we show that AID is not an interferon responsive gene and abrogation of Toll-like receptor signaling does not diminish the AID response. However, we found that NF-{kappa}B was required for expression of virally induced AID. Since NF-{kappa}B binds and activates the AID promoter, these results mechanistically link viral infection with AID transcription. Thus, induction of AID by viruses could be the result of several signaling pathways that culminate in NF-{kappa}B activation, underscoring the versatility of this host defense program.


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